Maternal riboflavin deficiency,resulting in transient neonatal-onset glutaric aciduria Type 2, is caused by amicrodeletion in the riboflavin transporter gene GPR172B
Gladys Ho(The University of Sydney), John Christodoulou(The University of Melbourne), Atsushi Yonezawa(Kyoto University Hospital), Rikke Katrine Jentoft Olsen(Aarhus University Hospital), Keow Giak Sim(Children's Hospital at Westmead), Gregory B. Peters(Children's Hospital at Westmead), Ken‐ichi Inui(Kyoto Pharmaceutical University), John J. Mitchell(University of North Carolina at Chapel Hill), William J. Rhead(Children's Hospital of Wisconsin), Kevin Carpenter(The University of Sydney), Satohiro Masuda(Himeji Dokkyo University)
Unknown
January 1, 2011
Cited by 0
Related Papers
Phenylalanine hydroxylase deficiency: diagnosis and management guideline
|Genetics in Medicine|2014|718
Survival after Treatment with Phenylacetate and Benzoate for Urea-Cycle Disorders
|New England Journal of Medicine|2007|357
Phenylketonuria Scientific Review Conference: State of the science and future research needs
|Molecular Genetics and Metabolism|2014|271
Targeted disruption of mouse long-chain acyl-CoA dehydrogenase gene reveals crucial roles for fatty acid oxidation
|Proceedings of the National Academy of Sciences|1998|254
‘Classical’ organic acidurias, propionic aciduria, methylmalonic aciduria and isovaleric aciduria: Long‐term outcome and effects of expanded newborn screening using tandem mass spectrometry
|Journal of Inherited Metabolic Disease|2006|247